Induction of arthritis in rats by aqueous suspensions of mycobacteria without the use of oil

Levine, Seymour; Saltzman, Arthur

doi:10.1002/art.1780340110

Cited by 7 publications

(3 citation statements)

References 16 publications

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“…AIA develops in susceptible rat strains after the injection of FCA (1)(2)(3)(4)(5)(6)(7)(8)(9). The first step in the development of AIA is the production of an immune response to FCA.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Cannon

Openshaw

Hibbs

et al. 1996

Arthritis & Rheumatism

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Objective. To investigate the role of nitric oxide (NO) production and NO synthase (NOS) induction during adjuvant-induced arthritis (AIA) and collageninduced arthritis (CIA) in Dark Agouti rats.Methods. Urinary nitrate excretion and immune NOS (iNOS) messenger RNA (mRNA) expression were measured in the joint, lymph node, spleen, and liver tissues following the induction of either AIA or CIA.Results. Urinary nitrate excretion and iNOS mRNA expression increased substantially during joint inflammation in both models of arthritis. However, the increases in urinary nitrate excretion and iNOS mRNA expression observed in the joint, liver, and spleen tissues during AIA were greater than those observed during CIA, although iNOS induction in the lymph nodes was similar for both models. A prior injection with Mycobacterium bovis heat-shock protein resulted in suppression of arthritis and NO production in AIA, but not in CIA.Conclusion. Differences in NO production during AIA versus CIA are a reflection of the fundamental pathophysiologic differences between these 2 models of arthritis. Thus, NO production in these 2 models could not be merely a nonspecific reaction to the adjuvant injection, nor simply a byproduct of local inflammation in the joint.Adjuvant-induced arthritis (AIA) and collageninduced arthritis (CIA) are different models of experi-..Supported by the VA Medical Research Program, the NIH (grants HL-40665 and HL-37615), the Nora Eccles Treadwell Foundation, and a University of Utah Research Grant.Grant W. Cannon, MD, Scott J. Openshaw, BS, John B. Hibbs, Jr., MD, John R. Hoidal, MD, Thomas P. Huecksteadt, Marie M. Griffiths, PhD: VA Medical Center, and the University of Utah, Salt Lake City.Address correspondence to Grant W. Cannon, MD, VAMC (llE), 500 Foothill Drive, Salt Lake City, UT 84148.Submitted for publication September 11, 1995; accepted in revised form May 1, 1996. mental arthritis that are induced by the injection of Freund's complete adjuvant (FCA) (1-12) or type I1 collagen (CII) (13-21), respectively. Although these 2 models have many clinical similarities, fundamental differences in their pathophysiology and genetic control are clearly evident. AIA is a particularly informative model because it predominantly involves T cell-mediated mechanisms (1-8), in contrast to CIA, which requires both humoral (14-20) and cellular immunity (21).Nitric oxide (NO), an unstable radical produced by the action of the enzyme NO synthase (NOS) on 1.-arginine, is a mediator of multiple physiologic functions and may also mediate local inflammation and tissue destruction (22-25). After its production and local action, NO is eventually oxidized to nitrate, which is inactive and excreted in the urine. Urinary nitrate can be reduced to nitrite, which, when measured by the Griess reaction, serves as an indirect measure of NO production (22). The induction of immunehflammatory NOS (iNOS) messenger RNA (mRNA) can be detected by polymerase chain reaction (PCR).Recent evaluations of NO synthesis in streptococcal cell wall...

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“…AIA develops in susceptible rat strains after the injection of FCA (1)(2)(3)(4)(5)(6)(7)(8)(9). The first step in the development of AIA is the production of an immune response to FCA.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Cannon

Openshaw

Hibbs

et al. 1996

Arthritis & Rheumatism

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“…The differences between DA rats and Lewis rats have been recently emphasized by the different characteristics of arthritis induced with rat collagen in these 2 strains (5) and the differences in susceptibility of these animals to aqueous suspensions of adjuvant (6). Other studies have also emphasized the varied arthritogenic responses among different rat strains (7,8).…”

Section: Discussionmentioning

confidence: 99%

Suppression of adjuvant‐induced arthritis in da rats by incomplete freund's adjuvant

Cannon¹,

Griffiths²,

Woods³

1993

Arthritis & Rheumatism

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Objective. To define the effects of incomplete Freund's adjuvant (LCFA) on subsequent arthritis induced by complete Freund's adjuvant (CFA) and type I1 collagen (CII) in DA and Lewis rats.Methods. ICFA was injected into DA and Lewis rats before CFA or CII injection.Results. DA rats previously injected with ICFA had significantly less severe arthritis induced by CFA compared with those not receiving ICFA pretreatment (P < 0.01). ICFA had no significant impact on CFAinduced arthritis in Lewis rats or on CII-induced arthritis in DA rats.Conclusion. The injection of ICFA alone specifically suppresses subsequent CFA-induced arthritis in DA rats, but not in Lewis rats. DA rats injected with incomplete MATERIALS AND METHODSAnimals. All procedures involving animals were approved by the institutional animal care and use committees of the University of Utah and the VA Medical Center. DA rats from Bantin and Kingman (Fremont, CA), DA rats bred in facilities at the University of Utah, and Lewis rats from Harlan Sprague Dawley (Indianapolis, IN) were used. All animals were male and were 8-12 weeks old at the time of study.Injections of incomplete and complete Freund's adjuvant. ICFA (Difco, Detroit, MI) was administered as 0.1 ml injected intradermally at the base of the tail (1-3). The same lot of ICFA was used in experiments 1,2, and 3. During each of experiments 4,5, and 6, different lots of ICFA were used. CFA was prepared by mixing Mycobucterium butyricum (Difco) and ICFA at a concentration 7.5 mg/ml. CFA injections (0.1 ml) were administered intradermally at the base of the tail.Induction of collagen-induced arthritis. Porcine type I1 collagen (CII) was prepared for injection as previously described (4). Briefly, CII was suspended in 0.1M acetic acid at 1 mglml and emulsified in an equal volume of ICFA (Difco) to give a final concentration of 0.5 mg/ml of CII in the emulsion of acetic acid and ICFA. Rats were injected intradermally on the back with 2 mg/kg CII. Arthritis evaluation. An observer who was blinded to the previous treatment evaluated the animals daily for the onset of arthritis and assessed the severity of arthritis twice weekly, as previously described (1-3). The severity of arthritis in the wrist, mid-forepaw, mid-hindpaw, and ankle joints was scored as 0 = no arthritis, 1 = extreme redness and/or minimal swelling, 2 = moderate swelling, 3 = severe swelling, and 4 = severe swelling and inability to bear weight. The presence or absence of arthritis in the interphalangeal, metacarpophalangeal, and metatarsophalangeal

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“…Increased absorption of antigen into the lymph nodes is likely to increase the immune response. Recently, it has been found that absorption of antigens and other materials from the peritoneal cavity of rats is increased during the healing (postinflammatory) phase of a chemical peritonitis [1][2][3][4], Subsequent enhancement of the immune response has been found in studies of hemagglutinating antibodies [5] and several forms of cellmediated immunity: graft-vs.-host disease and hostvs.-graft response [2], experimental allergic encepha lomyelitis and adrenalitis [2,[6][7][8][9][10], and adjuvant arthritis [11]. In the present work, enhancement of sys temic anaphylaxis has been produced by sensitizing or challenging rats in the postinflammatory state.…”

Section: Introductionmentioning

confidence: 99%

Anaphylaxis Is Enhanced by Increased Absorption of Antigen in Postinflammatory State

Levine¹,

Saltzman²

1991

Int Arch Allergy Immunol

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Hemagglutinating antibodies and cell-mediated immunity are increased when antigens are injected intraperitoneally (i.p.) into rats during the healing phase of a chemical peritonitis. In the present work, the anaphylactogenic effects of either sensitization or challenge were increased when any of three different antigens were injected i.p. in the postinflammatory state. The postinflammatory state made it possible to sensitize rats for anaphylaxis without any adjuvants at all. Lymph nodes draining the peritoneal cavity had evidence of enhanced absorption of inoculum in the postinflammatory state.

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Induction of arthritis in rats by aqueous suspensions of mycobacteria without the use of oil

Cited by 7 publications

References 16 publications

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Suppression of adjuvant‐induced arthritis in da rats by incomplete freund's adjuvant

Anaphylaxis Is Enhanced by Increased Absorption of Antigen in Postinflammatory State

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